In the past 10 months, we have demonstrated how an acute tracer-dose of 203 Pb is handled by the kidney. In stop-flow experiments we have, on anesthetized dogs, demonstrated that lead is reabsorbed by both the proximal and distal tubule. In renal clearance studies, also on anesthetized dogs, we have shown that trace amounts of 203 pb are readily filterable at the renal glomerulus (50-90 per cent) and that the filtered lead is largely reabsorbed, probably in the proximal tuble. The renal effects of EDTA on lead handling were largely to block reabsorption rather than increase filtration. In the next 12 months we plan: 1) to determine if chronic lead-loads are handled by the kidney in a manner similar to acute 203 Pb; 2) to study the renal adaptive mechanism in the handling of chronic lead loads of various magnitudes; 3) to characterize the ligand to which renal-ultrafilterable lead is bound; 4) to determine the effects of other chelators and other factors (e.g. PTH) on renal handling of lead; 5) to determine the effect of lead on renal-renin release; 6) to determine the effect of lead on renal release of erythropoietin.